Necrotizing fasciitis is a rapidly progressive bacterial infection characterized by necrosis of subcutaneous tissue and fascia, often accompanied by systemic toxic shock. This disease can be caused by a variety of bacteria.
Many bacteria can cause necrotizing fasciitis, which can generally be divided into two types.
Type I necrotizing fasciitis
Type I necrotizing fasciitis is a polymicrobial infection caused by anaerobic bacteria, aerobic bacteria, and facultative anaerobic Gram-positive and Gram-negative bacteria, up to 15 different pathogens that can be cultured in the infected focus, averagely 5 kinds of bacteria in a lesion. Most pathogens are derived from intestinal microflora, such as Escherichia coli, Pseudomonas, Bacteroides, and Vibrio. Risk factors include immunologic injury, recent surgical history, and possible abdominal lesions such as malignant tumors.
Type II necrotizing fasciitis
Type II necrotizing fasciitis is mostly a monomicrobial infection, often Gram-positive microorganism. The most common pathogen is group A hemolytic streptococcus. Single infection or infection in combination with other infections can also be caused by staphylococcus aureus. Necrotizing fasciitis without clear predisposing factors is more likely caused by streptococcus, and can also be community acquired methicillin-resistant staphylococcus aureus (MRSA) infection in recent years. Risk factors include contusion, laceration, burns, skin fissures, recent surgical history, childbirth, intravenous medication, and varicella infection. Patients without clear portal of entry may be caused by hematogenous transmission from the throat to the site of skin injury. The mortality rate of type II necrotizing fasciitis is very high, up to 50% - 70%.
Common risk factors include age >50 years, intravenous medication, and debilitating diseases, including diabetes, immunosuppression, obesity, and peripheral vascular disease. It is also increasingly realized that non-steroidal anti-inflammatory drugs may cause or aggravate necrotizing fasciitis. Non-steroidal anti-inflammatory drugs may conceal early signs and symptoms of necrotizing fasciitis, and may also inhibit neutrophil function, increasing cytokine release, directly causing necrotizing fasciitis.
Necrotizing fasciitis is a deep tissue infection that causes progressive destruction of the fascia of muscles and the covered fat. Because of the abundant blood supply, muscle tissue is often not involved. Infection usually spreads along the fascia of muscles, and signs and symptoms on the surface are usually absent. This feature makes it difficult to diagnose necrotizing fasciitis without surgery.
Although the pathophysiological mechanisms of type I and type II necrotizing fasciitis are the same, the clinical manifestations of the two types may be quite different depending on the pathogenic bacteria. Type I necrotizing fasciitis is usually chronic, can progress for several days, and is often secondary to abdominal surgery, peritoneal infection, or ischiorectal abscess. However, type II necrotizing fasciitis tends to progress more rapidly. The disease may occur in healthy persons without signs and symptoms. About 50% of patients with type II necrotizing fasciitis have toxic shock syndrome caused by exotoxins, which can significantly increase the mortality up to 67% from 40%.
In type II necrotizing fasciitis, a large amount of T cell proliferation and cytokine release can occur due to the action of the M protein of group A hemolytic streptococcus. This filamentous protein is anti-phagocytic and is an important virulence factor due to its ability to produce pyrogenic exotoxins with superantigen action, which can lead to systemic inflammatory reactions, causing multiple organ failure.
Signs and Symptoms
In the early stage, tenderness, severe pain, swelling, erythema, and elevated skin temperature can occur. When the sensory nerves in the lesion are destroyed, severe pain can be replaced by numbness or paralysis, which is one of the characteristics of the disease. In the medium stage, due to the destruction of nutrient vessels and vascular thrombosis, cutaneous paleness, cyanosis, and necrosis appear quickly. Discrete, different sized, bloody fluids filled vesicles or bullae occur on the surface of the skin. Severe cutaneous ischemia may occur. Pain may worsen and symptoms of systemic poisoning such as fever, dehydration, and apathy may occur. In the late stage, the skin is darkening, progressive and extensive necrosis and liquefaction of subcutaneous tissue, superficial fascia, and deep fascia occur, the exudate is bloody serous fluids with malodor, and severe complications such as shock, coagulopathy, and multiple organ dysfunction syndrome may occur.
Non-steroidal anti-inflammatory drugs can conceal changes of body temperature, pain, or numbness caused by nerve lesions in the late stage. When the underlying infection spreads to the subcutaneous tissue, the epidermis and various layers of the skin begin to swell, presenting orange peel skin and indurated wooden skin.
Diagnostic considerations include:
- Extensive necrosis of subcutaneous fascia and extensive undermining spread to the surrounding
- Severe systemic poisoning symptoms accompanied by altered mental status
- Involvement of muscular layer
- Clostridium not found in the blood culture
- Presence of vascular obstruction
- Extensive cell infiltration, focal necrosis of adjacent tissue of fascia, and microvascular embolization found in debridement
Finger test is considered to be the best method for the diagnosis. Under local anaesthesia, a 2cm incision down to the deep fascia can be performed. If the skin can be easily separated from the fascia along the interstitial space, the finger test is positive, and necrotizing fasciitis should be highly suspected.
Intraoperative direct vision of the fascia and subcutaneous tissue can assist in the definitive diagnosis.
Treatment of necrotizing fasciitis includes early debridement of necrotic tissue, use of broad-spectrum antibiotics, and hemodynamic support.
Necrotizing fasciitis is a surgical emergency and should be immediately surgically intervened. Evidences suggest that mortality can be as high as 100% if only antibiotics and supportive care are available. Surgery is the key method to remove the infected focus. The purpose of surgery is to remove all necrotic tissues.
Tissue specimens should be sent to the laboratory for Gram staining and culture. Patients should return to the operating room in 24 hours for reexamination and further debridement if necessary. In some cases, a very wide range of resections, such as amputations, are needed to effectively prevent the spread of infection.
Antibiotics are important for control of the condition, and early application can prevent the disease from developing into septic shock. The recommended treatment regimen is clindamycin plus meropenem plus vancomycin.
Immunoglobulin can be used as an adjuvant treatment. The recommended treatment dose is 2g/kg intravenously.
Hyperbaric oxygen therapy can increase the bactericidal effect of neutrophils, because the bactericidal effect relying on oxygen free radicals is greatly reduced in the case of hypobaric oxygen. Hyperbaric oxygen itself can also disinfect certain anaerobic bacteria, including Clostridium perfringens, because it blocks the production of α toxin. Therefore, hyperbaric oxygen therapy is believed to be helpful in the treatment of the infection.